AbstractThe infection process as well as the life cycle of Trypanosoma cruzi has been studied for many years; however, many cellular and molecular events involved in these processes have only recently been described and others remain unstudied. The process of infection of Trypanosoma cruzi is complex and surely involves the participation of many proteins; nevertheless, in very little experimental evidence exists that outlines the role of any given protein. The present work characterizes parasites that express an additional mutated copy of LYT1 , copy gene required for efficient infection. The mutant parasites displayed a phenotype similar to that of parasites carrying a LYT1 deletion. These parasites exhibited diminished infectivity and hemolytic capacity whereas their ability to cycle through the different developmental stages was enhanced. This phenotype is consistent with the behavior of a dominant negative mutation in which the product of the additional copy of altered LYT1 inhibits the normal function of native LYT1 protein or the protein complex it associates with.